QUESTIONS AND ANSWERS: Deer

Q: What are Chronic Wasting Disease and Tuberculosis and what
do they have to do with deer?

A: Chronic Wasting Disease (CWD) is a disorder of
the nervous system, and part of a group of diseases called Transmissible
Spongiform Encephalopathies (TSE’s). The TSEs include diseases of sheep
such as scrapie and the infamous ‘mad cow disease’ (bovine spongiform
encephalopathy), a variant of which is suspected to cause
Creutzfeldt-Jakob Disease (CJD) in humans. CWD is similar to BSE and
scrapie, but affects only cervids (deer and elk). The precise cause of
CWD was unknown until very recently. Some authorities had suggested that
CWD was caused by a bacterium, while others postulated that it could've
be an unconventional incomplete virus called a “virino”. However, more
recent data suggest that CWD is caused by an infectious abnormally
folded protein called a “prion”. Prions collect in the brain, causing
the death of brain cells and the formation of microscopic holes in the
brain tissues. These prions seem to be capable of resisting the enzymes
and chemicals that might normally breakdown infectious proteins. There
is an additional complication too, because infectious prions have the
ability to cause normal proteins to re-fold in their own image, leading
to rapid increase of infectious prion numbers.

CWD is always fatal, and there is normally a long incubation period
before the symptoms -- which include weight loss, behavioural changes
(i.e. isolation), blank facial expressions, nervousness, excessive
salivation, teeth grinding and repetitive patterns of movement --
appear. CWD is currently a significant problem in the deer and elk
populations of the United States. Wide-scale surveillance programs have
led to a decline in 'reactions' (i.e. animals testing positive for the
disease) in many parts of America, but recent lapses in surveillance
have led to an increase in some states (e.g. Alberta). Prior to the
introduction of such surveillance, and according to an article in The
Guardian newspaper, in the Rocky Mountains (Colorado) alone as many as
one-in-ten deer and one-in-twenty elk were thought to be infected. At
present, culling elk and deer, along with imposing fines for people
feeding them (as this draws deer from miles around, increasing the
potential for infection) are the only ways that authorities have found
to get a handle on the situation. Contrary to popular misconception,
there is currently no evidence that CWD can be transferred to humans,
although the consumption of meat from infected animals is not advised
and hunters are advised to take precautions when preparing/dressing
their carcasses.

Tuberculosis (frequently shortened to TB) is an infectious disease
that most often attacks the tissues of the lungs (although it is capable
of attacking any part of the body). The most common form of TB is caused
by the bacterium Mycobacterium tuberculosis, although there are various
other species and subspecies of Mycobacterium that can cause different
forms of TB.

Bovine TB has been documented in wild deer, the first incidence was
in a farmed animal during 1988, but cases are typically rare. In
Mammals
of the British Isles: Handbook, 4th Edition, Brian Staines and his
co-authors note that there is only a single ‘hot spot’ of bovine TB in
wild deer in southwest England where deer densities are unusually high,
and a single record from Scotland. Indeed, a survey of mammal carcasses
collected by the Food and Environment Research Agency (at the time known
as the Central Science Laboratory) in York confirmed bovine TB in 1% of
the Red deer specimens, although the report did conclude that Red and
Fallow posed the greatest threat of transmitting the disease to cattle
and that the gregarious nature of these species is likely to aid the
spread of the bacteria. The disease causes damage (in the form of
lesions) to the deer’s tissues, especially in and around the lungs and
lymph nodes – different species get different patterns of damage, which
in turn affects how the disease can be passed to other animals. A study
of the patterns of these lesions in 35 Red deer shot by hunters in
France led Gina Zanella at AFSSA (France’s equivalent to Britain’s
DEFRA) and her team of epidemiologists to conclude that Red deer were
more likely to spread the disease to other animals than were wild boar,
and the observation that deer react to bTB infection by forming
abscesses mean they are more resistant to the disease than wild boar,
making them a ‘true host’. Work by Andrew Paterson at DEFRA suggests
that the gross lesions associated with bTB in Red deer are an advanced
feature of the disease such that they can be infected with the
tuberculosis bacterium without showing any visible signs. Dr Paterson
has also observed that the features associated with bTB infection can
sometimes be confused with infection by other Mycobacterium species,
such as Avian TB and Jöhné’s Disease. Bovine tuberculosis is a
notifiable disease in Britain, meaning that by law even suspicion of
infection must be reported to the Local Authority and Health Protection
Agency. Curiously, however, there is currently no statutory surveillance
of TB in live farmed, park or wild deer of any species in Britain.

In their Handbook chapter, Staines and his co-workers go on to
point out that there are a ‘handful’ of bTB cases from Ireland. Indeed,
13% of Red deer culled in Northern Ireland between 1996 and 1997 tested
positive for the disease, as did nearly 3% of the 340 deer culled in an
Irish national park during 1997. Bovine TB seems more prevalent in deer
outside of the UK and a survey of Red deer and wild boar killed during
the 2001/02 hunting season in Normandy, France revealed that both
species were ‘heavily infected by M. bovis’.

Paratuberculosis (PTB), a chronic inflammatory disease of the
intestinal tract, has also been recorded in deer. The disease-causing
agent is the bacterium Mycobacterium avium paratuberculosis, which lives
in the intestinal cells and lymph nodes, causing progressive thickening
of the bowel wall of the lower intestine and the upper large intestine. PTB is an incurable wasting disease, variants of which affect humans and
livestock. According to a paper published in the Journal of Wildlife
Diseases during 2002 by a team of scientists at the Universitat Autonoma
de Barcelona, PTB was found in a population of about 1000 free-ranging
Fallow deer (Dama dama) between 1997 and 1998 in Spain. Five of the
eight deer studied had diarrhoea and lung lesions, and M. a. paratuberculosis was cultivated from two.

It should be noted that the incidence of TB in deer is very low, as
are records of deer carrying anthrax, foot-and-mouth disease and lime
disease. Bovine TB is currently a very hot topic in cattle and badger
biology. (Back to Menu)

Q: What are antlers and why do deer have them?

Short Answer: Antlers
are bony structures, distinct from horns, unique to deer and carried by
the males of most species – exceptions include the Chinese Water deer (Hydropotes
inermis) and the Musk deer (Moschus sp.), neither of which possess
antlers, and the Reindeer or Caribou (Rangifer tarandus) in which both
sexes grow antlers. Antlers grow from permanent outgrowths of the
skull’s frontal bone, called pedicles, and are covered by a layer of
hairy skin called velvet during their development. An increase in
circulating blood testosterone (usually at the end of summer in
temperate species) leads to a shedding of the velvet and reveals the
antlers in time for their use during the breeding season. Thus, in most
species, antlers develop while the testes are in a regressed state – the
exception is the Reeve's muntjac (Muntiacus reevesi), which remain fertile
throughout the year. The antlers are used by the stag to compete with
other males for the right to mate; in female reindeer it is generally
accepted that antlers allow them to compete for food during winter and
offer some protection to their calves. Once the breeding season is over,
a drop in circulating testosterone leads to the antlers being cast and
the cycle begins again. The antler cycle (i.e. when growth begins, when
shedding happens and when antlers are cast) is highly correlated with
the season and specifically photoperiod. Antler complexity increases
with age until the animal reaches senescence and the size/weight of the
antlers is closely correlated with body size. Older males cast their
antlers before younger stags and this may be at least partly because it
takes longer to grow larger, more complex sets. Antler size/weight is
related to habitat and especially food availability, although genetics
seems to be important when considering antler morphology. Failure to
grow pedicles will lead to an inability to produce antlers, while
hormonal imbalances (e.g. caused by testicular mutilation or castration)
can disrupt the development and lead to the production of deformed
antlers. There is some suggestion that parasite load may also be related
to certain antler deformities.

The Chinese Water deer (Hydropotes
inermis) is the only cervid species found wild in Britain in which
the males do not grow antlers.

The Details: Eighteenth century French naturalist Georges Louis
Leclerc de Buffon insisted that antlers were made of vegetable matter,
namely wood; given their appearance, this is perhaps understandable,
although it raises questions about how it got to be attached to the
deer’s head. Despite such initial misinterpretations, it was the
superlative French zoologist Georges Cuvier who established their true
nature in 1817. Put simply, antlers are bony organs grown by, indeed
unique to, deer. The first crucial distinction to make is the difference
between antlers and the appendages possessed by many other ungulate
species: horns. Despite some older texts using ‘antler’ and ‘horn’
interchangeably, there are significant differences between the two
structures. Horns and antlers start life in similar ways, as bony
outgrowths of the frontal bones (those that form the forehead). In
horns, however, this bony core becomes surrounded by a ‘sleeve’ of
material composed of fibrous structural proteins (largely keratin, the
strong protein found in your hair and fingernails); the sleeve continues
to grow -- with new material produced by modified cells at the base --
throughout the animal’s life, such that the horn becomes progressively
longer (and usually becomes twisted) as the animal ages. Antlers, by
contrast, do not grow directly from the skull and are replaced
periodically.

Before we consider the process of antler development, we need to
cover a little bone biology. Histologists typically class bone as either
immature (which occurs as part of embryonic development as well as in
the repair of fractures) or mature (which forms the skeleton of adult
mammals). Mature bone can then be classified as either cortical (hard,
compact bone with few spaces and a porosity of 5% to 30% – this makes up
about 80% of the adult human skeleton) or trabecular (sometimes called “cancellous”
or “spongy” bone owing to its network of rods and plates that gives it a
porosity of up to 90%). Cortical bone forms the outer layer (or ‘shaft’)
of a bone, while trabecular bone is the filling. In deer, as in most
other mammals, the forehead consists of paired frontal bones that are
composed largely of trabecular bone. In a 1973 paper to the Journal of
Embryological and Experimental Morphology, Gerald Lincoln demonstrated
that male Red deer (Cervus elaphus) foetuses receive a surge of
testosterone just prior to the sexual differentiation that occurs at
about 42 days old (i.e. up until this surge the foetus is neither male
nor female). It seems that once this differentiation has happened an
‘outgrowth’ starts to form on each plate just in front of the eye
sockets – these 'bumps' are composed of the same trabecular bone as, and
can thus be considered extensions of, the frontal bones. These
outgrowths are known as pedicles (from the Latin meaning ‘little foot’)
and Dr Lincoln observed that they appeared on Red deer stags about 60
days into development (i.e. during the second half of the gestation),
although subsequent growth of the skull caused them to become less
obvious as development progressed and they are imperceptible by about
115 days. Lincoln observed what he described as “opaque, slightly
raised areas in the position of the antler pedicle” on hind foetuses,
but these failed to expand in the same way they did in stags, presumably
because the females weren’t subjected to the same testosterone surge. In
many deer, it is a while after birth before the pedicles are visible
and, in his comprehensive review of the subject for Mammal Review in
1975, the late deer biologist Donald Chapman wrote that:

“... in Fallow and Red deer in southern England, pedicles could not be
felt in newly-born male animals and the skulls of many six-month-old
male animals showed no sign of pedicle development ...”

Red deer skulls. The top photo shows
a stag's skull (illustrating extension of the skull into the pedicles,
from which the antlers develop). The bottom photo shows a hind skull -
notice no skull extensions.

It appears that, as with so much of a deer’s development, the quality
of the habitat strongly influences when the pedicles begin to grow and
by when they have completed their development – several authors have
noted that Red deer in the high quality environment of a deer park can
have pedicles by three months old, while those on the impoverished
hillsides of Scotland may not have functional pedicles until their
second or third year. On average, Red stags in the wild will begin
antler development at about 10 months old. Fallow (Dama dama) and Sika (Cervus
nippon) deer living in favourable conditions tend to begin antler
development at 11 to 15 months old, while Roe (Capreolus capreolus)
usually start sooner. In his 1995 book The Roe Deer, Richard Prior notes
that Roe bucks have palpable pedicles by three months old; these
pedicles can be seen with the naked eye come September (about four
months old) and, if well fed, the buck often has small antlers (called
‘buttons’) by January at the age of about eight months. Earlier authors
have recorded remarkably precocious antler development in Roe deer, with
buttons complete by four months old! Muntjac deer (Muntiacus reevesi)
have observable pedicles by about five months old, with antlers grown
from May to September. In his Mammal Review paper, Dr Chapman notes that
as a general rule of thumb, the Telemetacarpalian deer (e.g. Roe – see
Deer Taxonomy) begin antler development in the autumn of their first
year, while the Plesiometacarpalian species (e.g. Red, Sika and Fallow)
don’t start until early in the year following the year of their birth. Regardless of when development begins, the first antlers are usually
simple, un-branched spikes (only in exceptionally well-fed animals are
they sometimes branched) that grow as extensions of the pedicles and
consequently lack the elaborate base -- called the coronet or
burr --
that mature antlers have.

The basic anatomy of antlers
(modified from Putman, 1988). The top image shows a typical Red deer (Cervus
elaphus) antler, while the bottom depicts the antler of a Fallow
buck (Dama dama).

Growth and development
The precise mechanisms by which the pedicles
form, and the various ‘growth zones’ and processes within the developing
antler are outside the scope of this article, but readers interested in
a technical appraisal are referred to the papers listed at the end of
this section – that which follows is an amalgamation from these sources.
The basic development can be divided into two stages: the initial
formation of the pedicle and the growth of the antler on top of it.
Histological studies have found that it is the membrane that surrounds
the pedicle, the periosteum as it is known, that is crucial in
permitting antler formation. In a series of eloquent, if somewhat
Frankensteinian by modern standards, experiments German anatomists
Hermann Hartwig and Josef Schrudde demonstrated that transplanting the
section of the periosteum overlying the pedicle of a Roe deer fawn to
its metacarpus resulted in an antler being grown on the deer’s foreleg.
Several years after these studies, Richard Goss at Brown University
named this tissue ‘antlerogenic periosteum’ (abbreviated to AP), which
roughly translates to ‘antler-producing bone cover’. The pedicle begins
life as a small section of AP tissue; the cells are spurred into
differentiation (i.e. turning into antler-forming cells) by a rise in
the levels of testosterone in the blood. As the cells multiply and the
area grows in size, minerals (predominantly calcium and phosphorous) are
deposited through a process known as mineralization. Mineralization is
one of the steps in the process of turning a tissue into bone; a process
called ossification. In a brief paper to the Journal of Zoology in 1986,
Norma Chapman described how, as the antler (in this case of Red deer)
grows, mineralization advances as a discrete band about two-to-four centimetres (about 1.5 in.) behind the growing apex.

Longitudinal cross-section through an
active pedicle showing the basic structure and growth zones (modified
from Price et al., 2005). The pedicles form as extensions of
the frontal bone and appear as 'bumps' on the deer's forehead.

The pedicle is surrounded by a dense hairy skin -- modified from that
on the scalp -- called velvet; in Roe deer this skin is covered with
longer hairs than found in other species, which are presumably an
adaption to growing antlers during the winter. The pedicle remains a
permanent feature of the animal’s skull, although it appears to vary in
width throughout the deer’s life (growing up until the deer reaches
senescence, at which point it begins shrinking) and there is some
suggestion that one pedicle may remain larger than the other. It
appears, incidentally, that the pedicle enforces some degree of polarity
on the antler and in 1991 Richard Goss found that if you cut a disc of
the AP, rotate it 180-deg, and put it back in the same place the antler
grows back-to-front. Once the pedicle reaches a ‘threshold size’ (this
seems to correspond to a body weight of about 30kg, 66 lbs, in Red deer)
additional bone formation begins at its tip.

The antler starts life as a small lump of mesenchymal tissue (i.e. a
loosely connected lump of, unspecialized cells) at the tip of the
pedicle called a blastema. The blastema is the site of active mitosis
(cell division) within the antler; cartilage is laid down that will
later be mineralized and ultimately ossified. This means that the antler
grows from its tip rather than from its base (as horns do), as
demonstrated in an elegant experiment by Herbert Bruhin during the
1950s. Bruhin inserted a screw 3.5cm (just under 1.5 inches) from the
antler base and another one 1.5cm (just over half-inch) from the antler tip
and, eleven weeks later, the first screw was still 3.5cm from the base,
but the second screw was now 5.5cm (just over 2 in.) from the tip.

Cross-sections of a cast antler
showing the bone layers. On the left is a lateral section through the
main beam showing the trabecular bone core, surrounded by the denser
cortical bone. The right shows a section through the brow tine, showing
the increasing cortical bone at the antler tip.

There are two main processes going on under the velvet as the antler
grows: cartilage in the core is ossified to trabecular bone (this is
called endochondral ossification), while the membranes surrounding the
core get turned directly to cortical bone in a process known as
intramembranous ossification. In other words, the antler grows in height
as more cartilage is produced in the core and turned to bone and it
grows in thickness as more compact bone is laid down around the shaft.
While the antler is growing it needs nourishment, in the form of
minerals and oxygen, which is receives from branches of the superficial
temporal artery (STA) – in humans, these are the major vessels that
break away from the carotid artery just in front of the ear and ascend
towards the forehead (when this vessel enlarges, it can result in a
migraine). As Dr Chapman notes in his review -- in Fallow, Sika and Red
deer -- the STA branches into about a dozen smaller arteries, each with
narrow interiors and thick walls, which ascend the antler and the
surrounding velvet. Chapman goes on to say: “The flow of blood
through the velvet is probably both copious and rapid judging from the
warmth of the growing antler tips.”

Top left:
Cross-section through the palmate (flattened) section of a Fallow buck's
antler - the image above shows a lateral section through the palm
looking down towards the coronet (Click here for clarification).
Bottom left: The main beam of the
Fallow antler showing the groves (or 'gutters') where the veins in the
velvet ran. Right: a longitudinal
section removed from the palm, illustrating how the trabecular bone
extends out within the palm. It is the amount of trabecular bone within
the core of the antler that means they're relatively light, given their
composition and size.

As the breeding season approaches, levels of testosterone in the
deer’s blood start to rise and this triggers substantial ossification at
the coronet, leading to a restriction of blood flow and a ligation
(‘tying off’) of the velvet. The connection between rising testosterone
and velvet shedding was established by scientists in the 1970s, who
found that castrated stags grew normal antlers but failed to shed the
velvet. When the blood supply to the velvet is shutdown the tissue dies
and begins to dry up and fall off – at this stage, the stag or buck is
said to be ‘in tatters’. The deer are often seen thrashing their antlers
in undergrowth, on bushes and on trees in a bid to remove the velvet in
a process known as cleaning or polishing – the decaying tissue may also
attract flies that can alight on the antler in such numbers as to turn
the antler black. When the velvet first peels the antlers are white
bone, but thrashing and rubbing against vegetation and soil causes
staining, which gives them a rustic colour anywhere from black, through
most shades of brown to grey. A stag or buck with cleaned antlers is
often said to be in the misnomer of ‘hard horn’.

Velvet skin covering the antlers of a
Red stag (left) and a Roe buck (right). Note that the hairs on the Roe
velvet are longer than those of Red antlers. Red velvet photo from
Wikipedia Commons, by Mehmet Karatay.

Once the velvet has been shed the antler is generally considered
‘dead bone’, because it is unable to grow any further or repair any
breakages. As deer biologist Richard Goss pointed out in 1992,
however, “nowhere else in nature is dead bone tolerated in an animal, in this
case from three to nine months, depending on species”. This got Hans
Rolf and Alfred Enderle at the University of Goettingen in Germany
thinking about whether the bone really was dead. In a fascinating 2002
paper to The Anatomical Record they presented their study on the vascularisation of Fallow deer antlers. Rolf and Enderle found that
even after the velvet had been shed the antlers were still being fed by
a series of capillaries and vessels from the pedicle; in other words the
antlers had a functioning vascular system that kept them moist, meaning
they were actually living bones. It appears that final mineralization of
the coronet may not happen until only a couple of weeks before the
antler is cast, at which point the bone cells effectively starve and the
antler ‘dies’. Indeed, a study of Roe deer antlers in the late 1980s
suggested that mineralization may continue well into the rutting season,
while data from Fallow antlers imply that some remodelling of bone may
occur even after the antler is fully mineralized. Of course, the
discovery that the antler is actually a living bone does not mean that
it is also a sensitive bone. The developing antler gets its nerve supply
from branches of the trigeminal nerve (the branches that serve the ears
and eyes) but this connection appears to die back with the velvet and
there is no evidence to suggest that the antler retains a nervous
connection once the velvet has been shed; breakage of the antler
certainly doesn’t appear to cause the deer pain.

The cast antler of an immature Fallow
buck. The red line denotes the cross-section displayed in the bottom
left of the image (the arrow shows the direction of view), which
illustrates two 'trabecular zones' that correspond to the mainbeam (on
the left) and the brow tine (on the right).

The high levels of circulating testosterone causes the antlers to be
retained for several months; throughout the breeding season and well
into the following year in many species. The final coronet ossification
(as described above), and ultimately the shedding (known as casting) of
the antlers, is triggered by a drop in testosterone in spring.
Histologically, it appears that just prior to casting, a zone forms at
the top of the pedicle (often betrayed by a swelling of the skin at the
base of the antler) where the bone is broken down by osteoclast
(literally ‘bone breaker’) cells – this process is called osteoclastic
resorption. This destruction of bone leads to a weakening of the
coronet-pedicle junction and the antler loosens and falls off. In his
1992 opus, The Whitehead Encyclopedia of Deer, G. Kenneth Whitehead
wrote that: “The loosening of an antler, prior to shedding, would appear
to be very sudden, and at the critical moment final separation of the
antler from the pedicle may be caused by the head being jarred on
landing following a jump over an obstacle.” Indeed, several authors have
noted how antlers close to being cast don’t wobble (as our teeth do
before we lose them), so osteoclastis presumably occurs rapidly. It
appears that the osteoclastis is considerable and, in 1992 review on the
biology of antlers, Gerald Lincoln noted how, if casting is prevented
(by hormone injection) the die-back progresses down the pedicle into the
skull and can be fatal.

Deer are often said to have cast their antlers simultaneously if both
are lost within 24 hours; when one antler is lost more than 24 hours
after the first it is referred to as asynchronous casting. Despite the
terminology, the antlers are very seldom cast in a truly simultaneous
manner and they can be shed anywhere from a few minutes to several
hours, even days, apart. Once an antler has been cast, the deer is left
with an open wound on the top of the pedicle; interestingly, there is
generally little blood loss and remarkably few cases of reported
infection. The wound healing process on the pedicle is exceptionally
rapid and, within hours of casting, the pedicle will have been covered
by a scab and new velvet will be growing over it. Histological studies
by German anatomist Uwe Kierdorf (at the University of Hildesheim) and
others have demonstrated that, under this newly-formed skin there is a
brief period during which more bone is broken down, giving the pedicle a
smooth surface, before bone growth resumes and the antler regeneration
process starts over.

Yearling = CalfSecond Year = BrocketThird Year = SpayadFourth Year = StaggardFifth Year = StagSixth Year = HartSeventh + Year = Great Hart

The age of the deer: The table above
gives the names assigned to deer of different ages, often based on the
development of their antlers.

A mature Red stag may well have 12 to 15 branches (called tines or
points) to his antlers and stags are often named according to the number
of these points. Deer with their first set of short, simple, unbranched
antlers (i.e. at two years old) are referred to as prickets (Fallow)
or brockets (Red - see
below, left). Over subsequent years,
the antlers should become progressively larger and branched (up until
the stag is about 10 years old, after which the number of tines starts
to decline). A Red deer with 12 points (six per antler) to his antler is
called a Royal stag, while 14 points make an Imperial stag and an animal
with 16 points or more is referred to as a Monarch. In his article for
South Coast Today (a Massachusetts news and current affairs website),
outdoor writer Marc Folco describes how hunters speak in terms of
“pointers”. Mr Folco explains that a deer with five tines each side is a
five-pointer, while one with six either side is a six-pointer. In cases
where the antlers are asymmetrical (i.e. different number of tines each
side), the two values are given separated by an “X” – thus, a deer with
six tines on one antler and five on the other is a “6 X 5”, rather than
an 11-pointer. In Fallow bucks, the palmation extends with subsequent
antler sets as do the number of points, called spellers in this species.

That time of the month
How do we know it’s testosterone that
regulates the antler cycle? Moreover, what controls the changes in
testosterone? It was Greek philosopher Aristotle who first noticed that
the genitals had an important connection to the development of antlers
and, around 350 BC, he wrote in his Historia Animālium that: “If stags
be mutilated, when, by reason of their age, they have as yet no horns,
they never grow horns at all; if they be mutilated when they have horns,
the horns remain unchanged in size and the animal does not lose them.” It would be several centuries until Aristotle’s musing would be
confirmed experimentally when, in 1913, two German anatomists
established that castration of a deer with cleaned or polished antlers
led to casting and growth of new antlers from which the velvet is never
shed. Subsequent experimentation by Richard Goss found that both
androgens (testosterone) and oestrogens (oestradiol) were able to
prevent old antlers from being shed, inhibit the growth of new antlers
and cause the velvet to shed prematurely from growing antlers. It has
also been shown that castration of a stag growing antlers prevents the
antlers from becoming completely calcified and the velvet from being
shed; the result is that the antlers may continue to grow and lead to
what Donald Chapman describes as “antler monstrosities”, including the
benign tumours that Dr Goss called ‘antleromas’. Studies by various
authors -- especially the Red Deer Research Group on Rum and Goss --
during the 1970s and 1980s provided further confirmation that
testosterone was the regulator; it was found that fitting castrated
stags with testosterone implants allowed them to resume a normal antler
cycle and testosterone injections initiated pedicle development in
females.

The question of what regulates testosterone is less straight forward
to answer, although for temperate deer at least (equatorial deer appear
to be a special case, as will become apparent) light is critically
important. More specifically, it is the number of hours of light and
subsequent darkness that the deer receives – this is referred to as the
photoperiod and expressed as light:dark ratio, such that 12L:12D would
mean 12 hours of light followed by 12 hours of darkness. Temperate deer
are highly seasonal animals and their biological (or circadian) rhythms
are heavily influenced by the changing daylength. Melatonin, the
so-called ‘hormone of darkness’, is produced by the deer’s pineal gland
in response to darkness and the more hours of darkness the animal is
exposed to, the more melatonin is produced. There are some ambiguous
data about the role of melatonin on sex hormones in mammals,
particularly humans at the moment, but in short-day breeders (i.e. animals that breed during the winter) it seems that gonadal functions
are activated by an increase in melatonin. Thus, an increase in
melatonin indirectly stimulates the testes to increase their production
and secretion of testosterone. The increase in circulating testosterone
then terminates bone formation in the antler and triggers the death of
the velvet. Indeed, biologists at Aberdeen’s Rowett Research Institute
reported, in a paper to the Journal of Reproduction and Fertility during
1986, that melatonin is a key hormone in regulating the antler cycle;
they demonstrated that velvet shedding and rutting could be induced up
to five weeks early in a stag given feed pellets containing the hormone.

The importance of photoperiod on antler cycle has been recognised for
more that half a century when, in 1954, Polish biologist Zbigniew
Jaczewski demonstrated that Red deer could produce two sets of antlers
in a single year if exposed to a ‘sped up’ photoperiod. Despite these
initial results the ways in which photoperiod regulated antler
development was, and to an extent still is, poorly understood. A series
of classical experiments on Sika deer conducted by Richard Goss at Brown
University in Rhode Island, however, improved our understanding. During
the seven year study, captive deer were held under the artificial
conditions of Brown University’s Animal Care Facility, where the
photoperiod and temperature were strictly controlled – the idea was to
expose the deer to various combinations of light and dark and see what
effect it had on their antler cycle. Goss found that, if the
photoperiod was reversed (i.e. the deer thought it was winter when it
was actually summer) they cast and re-grew their antlers six months
out-of-sync with the outside world. It was also possible to corroborate
and expand upon Jaczewski’s studies. Goss demonstrated that, if
the photoperiod was reduced to replicate a shorter year, the deer could
be made to regenerate up to four sets of (albeit stunted) antlers in a
single calendar year. Interestingly, Goss observed that when the
photoperiod was set to mimic six ‘years in one’ the deer didn’t produce
six sets of antlers, instead they returned to their normal circannual
cycle (i.e. one set per year); likewise when the photoperiod was
increased (making one year last for two) the deer still cast their
antlers each calendar year as normal. Overall, Goss concluded that
all the time the deer could entrain to (determine) the photoperiod they
could cast and re-grow their antlers accordingly, even if this led to
increased or irregular production. If, however, the photoperiod was one
that they couldn’t determine they simply reverted to their usual
circannual rhythm of casting and renewal. In other words, there is a
limit to the photoperiod that deer can adapt to.

Before we leave the subject of photoperiodic control of antler
cycles, we should give some consideration to deer living in equatorial
regions, where there are no seasons. Equatorial deer can be found with
antlers at any time of the year, but curiously many (although not all)
seem to cast annually, so they must have a method of keeping track of
time; precisely how this is achieved is still enigmatic. Dr Goss’ work
has shown us that there is something peculiar about an equinoxial
photoperiod (i.e. 12L:12D), his deer cast normally when given 12L but
fewer dark hours and vice versa, but when given 12L:12D they failed to
cast and casting was abated for up to four years in one animal. At
first, Goss thought it might have been the L:D ratio of one that
caused it, but exposing the deer to shorter durations of the same ratio
(i.e. 5L:5D, 6L:6D, 8L:8D and so on) caused the deer to cast as normal,
so there was something special about 12 hours of light followed by 12
hours of darkness that caused disruption to the cycle and a failure to
cast. We still don’t know what happens or how equatorial deer manage to
keep track of the year, although there is the suggestion that they are
sensitive to how many alternating periods of light and dark they
experience and associate a certain number with one year. Goss’ work
has provided interesting data to suggest that deer may at least be able
to keep track of photoperiods. By splitting deer into two groups and
exposing one to a regular short-day to long-day photoperiod (i.e. 4L:20D
to 20L:4D) and the other to the opposite, Goss found that antlers
were shed and re-grown in synchrony with every alternative change in day
length, regardless of the direction (i.e. lengthening or shortening) of
the change. In other words, it didn’t matter whether the days got longer
or shorter, the important thing was that the deer registered that there
had been a switch in the photoperiod and because the deer would normally
experience two shifts per year, they adjusted their cycle to shed every
second change. Given what we know about the function of hormones in this
cycle, it’s difficult to see how it could only be the number of shifts
in photoperiod that a deer registers as opposed to the amount of light
the shifts bring, which would have a direct stimulatory or suppressive
impact on melatonin production.

So, in the end, we have a cycle of bone growth and loss that is under
the control of light; light stimulates the production of melatonin,
which probably acts on the anterior pituitary stimulating the testis to
produce (or stop producing) the testosterone that regulates the
deposition of bone within the antler, and the blood supply to the velvet
surrounding it. The next step is to address what controls how the
antlers look and how large they grow.

A 'Royal' Red stag, with 12 antler
points, in the New Forest, Hampshire.

All shapes and sizes
For centuries the size of a deer’s antlers has
been of interest to humans and there are many collections of deer
antlers and heads around the world – the largest collection of
White-tailed deer (Odocoileus virginianus) heads, for example, currently
resides in the Buckhorn Hall of Horns in Texas. In years gone by Red
deer were transported from English parks to the hillsides of Scotland in
a bid to improve the quality (body size and ultimately antler size) of
the native stock; this implies an element of supposed genetic control
over the development of antlers. Indeed, many have commented that it is
possible to identify a stag over successive years by the shape of his
antlers; the Red Deer Research Group on Rum have apparently become
rather adept at this. The evidence, however, is far from unanimous and,
in his book The Roe Deer, Richard Prior wrote: “A buck’s age, let alone
his identity or his value as breeding stock, cannot be judged by his
antlers alone.” It is actually translocation studies that have shown us
that how large a deer’s antlers grow is not solely a reflection of
genes; diet is a crucial factor. In his Whitehead Encyclopedia of Deer,
G Kenneth Whitehead described how Scottish hill stags (which are
typically rather small-antlered animals) transferred to superior habitat
-- a deer park, for example -- are capable of producing antlers
comparable to stags in other high quality habitats, such as deciduous
woodlands. Indeed, Prior stated that it was habitat, rather than
bloodline, that had overriding influence on the antler size of Roe deer.
In his A Life for Deer, vet John Fletcher made much the same point when
he said: “undoubtedly the limiting factor in the productivity of
Highland red deer is very rarely the genetics of the deer but rather the
environment: food and shelter”. There are other population studies,
largely on Rum, suggesting that the average antler size declines with
increasing population density – more deer means more competition for
food such that each animal typically gets less, is in poorer condition
and thus produces smaller antlers. The Rum biologists have also found
that the weather and early life-history of the deer can also affect the
length of their first antler set – as may be expected, light calves born
late in the year and growing up in bad weather (mainly low temperatures)
developed smaller antlers than heavier calves born during good
conditions.

Despite a considerable body of evidence implicating habitat quality
in regulating antler size, this doesn’t mean that genetics are
unimportant. Ultimately, all structures in the body are built according
to the ‘blueprint’ laid out by the genome and it is well established
that there is a species-specific pattern to antlers (i.e. you can tell
the species of a deer by looking at its antlers), which is presumably
encoded in their genes. Indeed, we now have several studies showing that
there is a degree of heritability in both size and, perhaps more
importantly, shape of the antlers; the researchers on Rum estimate that
antler size is roughly 20% heritable. Overall, the data suggest that,
where food is not limiting and hormonal aberrations (accidental
castration, etc.) are absent, genetics play a fundamental role in
determining how large and into what shape a given set of antlers will
grow. When dietary and hormonal aberrations are encountered, these can
override the impact of the genes because such secondary sexual
characteristics (i.e. attractive features that aren’t necessary for the
physical act of reproduction) generally have low growth priorities. It
has also been established that a deer’s antlers become progressively
larger (in height and thickness) and more branched as the animal ages,
although there does not, however, appear to be a correlation between the
age of a deer and the number of tines on its antlers.

The understanding that antler size and complexity increases
throughout the stag or buck’s lifetime explains why it should be
necessary to cast the antlers they have invested so much energy growing.
The sensitive velvet skin is necessary for the antler to develop, but
must be removed before the antler can be used in combat. Removing the
velvet, however, effectively ‘kills’ the antler (despite some bone cell
activity the antler cannot grow or heal). Thus, if the antlers are to
grow with the deer’s body, it becomes necessary to replace them
regularly. As we shall see shortly, antler size and complexity appear to
help females judge how ‘fit’ a stag or buck is, as well as potentially
letting other males decide whether he’s worth fighting with. Thus, if
the antlers were never replaced, the male would either spend his entire
life with simple spikes that said nothing about his reproductive
prowess, or would need a set that were impracticably large for a
yearling to carry. All this casting and re-growing, however, doesn’t
come without a price. (Photo: Reeve's
muntjac antlers. Note the pedicles are much larger than those of other
species, being roughly the same length as the antlers. If you're unsure
where the pedicle stops and antler starts, hover your mouse over the
image to highlight the coronet.)

The cost of antlers
Antlers come in all shapes and sizes, from the
small (10cm / 4 in.) simple spikes of the muntjac (Muntiacus reevesi) to
the 1.5m (5 ft) organs sported by American wapiti (Cervus canadensis).
Moreover, we have seen that antlers are grown quickly. Indeed, they are
the fastest growing mammalian tissue; they exhibit a typical sigmoidal
growth curve (i.e. start slowly, speed up and then slow down just prior
to cleaning), growing several centimetres per day during their peak
growth period, and are complete within 12 to 16 weeks. Such rapid growth
requires a considerable amount of minerals, namely calcium and
phosphorous. In 1985, Paul Muir and his colleagues at the University of
Canterbury in New Zealand calculated that a Red stag producing three
kilos (just over 6.5 lbs) of hard antler deposits just over half-a-kilo
(19 oz.) of calcium and up to one kilo (just over 2 lbs) of other
minerals; during the final ten weeks of development (when growth is at
its most rapid), calcium is deposited at a rate of around 5g (1/5 oz.)
per day. This corresponds well with values given by Donald Chapman who,
in his Mammal Review article, notes that antlers are composed of about
50% minerals (the rest is largely ash and protein) and, of this, 45% is
calcium and 19% phosphorous. So, as Chapman points out, for an
‘average’ Red stag producing a pair of antlers weighing around 13kg
(just under 3 lbs) in 130 days, this means that the deer must produce an
average of 100g (3.5 oz.) of bone per day.

So, how do the deer find such large quantities of bone growing
minerals in such a short time? There is some evidence that minerals can
be sequestered internally, from the deer’s skeleton. Work by biologists
in the USA -- on Mule deer (Odocoileus hemionus) in the Rocky Mountains
of Colorado and Reindeer kept at Washington State University, to name a
couple -- has documented a decrease in bone mass, caused by osteoporosis
or osteoresorption. The researchers have recorded minerals being removed
from the skeleton, with the ribs and long bones (e.g. the metacarpus and
tibia of the legs) yielding a combined decrease in density of almost
60%; the bulk of this resorption seems to occur during the middle of the
antler’s growth period. It seems that, where resorption occurs, it is
more common in trabecular bone than in cortical bone, probably because
the former is more metabolically active.

Cast antler from a mature Fallow
buck. The extent of the palmation and the number and size of the
spellers ('finger fringes') increase with the age and condition of the
buck.

Obviously there is a limit to the amount of minerals that can be
sequestered from the skeleton, before the bone becomes too brittle to
support the animal; it seems unlikely that the complete antler set could
be constructed in this way. This is even more apparent when we consider
that antlers are allometric organs, which means that larger deer sport
larger antlers even after correcting for body weight. Consequently, deer
must get some of their minerals from their diet and one very good source
is antlers. Bone (and specifically antler) eating is apparently a fairly
common behaviour in deer and cast antlers represent a substantial
‘mineral bank’ – I have even come across reports of deer chewing on
another’s antlers while still attached! In their 1982 Red Deer: Behaviour and Ecology of Two Sexes, Tim Clutton-Brock, Fiona Guinness
and Steve Albon note that both stags and hinds on Rum chewed bones and
cast antlers, especially during the spring and early summer (when stags
are in velvet). In a fascinating paper to the journal Mammalia during
1985, Cyrille Barrette described the antler eating behaviour of wild
Axis deer (Axis axis) in the Wilpattu National Park, Sri Lanka. Prof.
Barrette witnessed 102 instances of osteophagia (literally ‘bone
eating’) during his two years of fieldwork, with all ages and both sexes
indulging – it was, however, the males in velvet that were seen to chew
bones most often. Apparently chewing bouts were fairly lengthy, lasting
on average nearly 40 minutes, if the ‘chewer’ wasn’t disturbed; in some
cases the antler was chewed down to the coronet! Describing the chewing
behaviour, Barrette wrote:

“In most cases, the deer did not pick up the bone off the ground but
only lifted the sharper end, chewing it with molars and premolars in the
‘cigar-like’ manner described by Sutcliffe (1973). The heavier end of
the bone rested on the ground and saliva could be seen dripping while
the animal worked the bone in its mouth”

Deer-chewed antlers collected by
Prof. Barrette during the aforementioned study. The top set are an
intact and chewed antler from an Axis deer (Axis axis), while the bottom
examples are from a Sambar deer (Rusa unicolor). In both cases, deer
have chewed the antlers almost down to the coronet. Photo used with
permission.

Incidentally, as something of a side-line, the reason that we don’t
find ourselves swimming in cast antlers when we go walking in the woods
(in fact, they’re pretty scarce) is probably because many are eaten by
deer and rodents. Where antlers are found, it is not uncommon to find
scrapes and indentations on their surface characteristic of having been
gnawed by one or more rodents and, in a brief communication to the
journal Science in 1940, former University of Toronto zoologist Alan F.
Coventry told of a Red squirrel (Tamiasciurus hudsonicus) regularly
visiting a moose skull outside his cabin on an island in Ontario’s Lake
Temagami, to gnaw at the bony projection. (Photo:
A typical gnaw mark, from a rodent, on a Fallow antler.)

Given the need for replacing antlers each year and the significant
metabolic drain involved in doing so, why should the deer go through all
this? What do they use these antlers for?

Swiss Army antlers
The function of antlers has long been a subject of
debate, with suggestions ranging from the lucidly apparent to the rather
bizarre. In 1937, for example, the eminent German zoologist Han Krieg
suggested that antlers were a method of removing excessive minerals
consumed in the diet. Today, there is little contention over the purpose
antlers serve or the reasons for their evolution. Before we look at the
currently accepted theory of purpose, let’s take a moment to look at
some of the competing ideas.

One thing we can be fairly certain of is that, given the high
energetic cost associated with growing antlers, if deer didn’t have a
good ‘reason’ for doing so, they almost certainly wouldn’t. Nature is in
finite balance and animals that waste their energy on frivolous organs
are lost from the population. Consequently, having antlers must convey
an advantage that is genetically heritable – in other words, having
antlers must make it more likely that you’ll survive and reproduce,
thereby sending your genes (which also contain the instructions for
building antlers) into future generations.

In a short paper to the journal Nature during 1968, Bernard Stonehouse at the University of Canterbury suggested -- based on various
anatomical observations, including the large number of blood vessels,
lack of fat under the skin and branching that provides a large surface
area -- that: “Thermoregulation may thus be the function which primarily
determines the form and proportions of antlers, and necessitates their
annual renewal”. In other words, antlers might have evolved to help deer
regulate their temperature by dissipating heat like the ears of an
elephant. The immediate problem with this idea, you might be thinking,
is that generally only males grow antlers; surely if it was a heat loss
adaptation females would grow them too? Well, Stonehouse argued that
males have a bigger problem losing heat because they put on weight more
rapidly (and maintain larger fat reserves) than females during the
summer months. In his review of the function of antlers
published in Behaviour during 1982, however, Tim Clutton-Brock suggested that the
anatomical peculiarities that Stonehouse listed were perhaps better
explained as a means to allow rapid growth of the antlers. Clutton-Brock
also pointed out that, not only do some deer grow antlers during the
winter (the Roe deer, for example), when they presumably have little
need to lose excessive heat, but also that: “in tropical cervids there
is no close association between antler growth and temperature” and “the
antlers of temperate deer species tend to be larger, relative to their
body size, than those of tropical species”.

An alternative suggestion was that antlers evolved as a method of
defence against predators. This was first suggested by Charles Darwin in
his 1871 book The Descent of Man and this may well be part of the story
although, as Dr Clutton-Brock pointed out, it seems unlikely that
antlers evolved principally as a means of defence given that only one
sex grows them. Indeed, females and their young are arguably more
vulnerable to attack by predators during the summer months than
stags/bucks are. That said, it is interesting to note that Reindeer
females grow antlers during the calving season and, unlike many deer
species, the calves accompany their mother as soon as they can walk
rather than being left lying in cover while the mother feeds. It seems
likely that antlers could allow the female to offer an extra element of
protection to her calf.

Some authors have suggested that antlers may have evolved as a tool
for gaining access to food. Indeed, Reindeer have been seen to dig
craters in the snow with their antlers to get at lichens and there are
various reports of deer using their antlers to knock fruit from trees
and even operate farm equipment to cut themselves some carrots. On reflection,
however, it seems unlikely that such tasks would require antlers of
increasing size and complexity and a more likely explanation is that the
antler can be used to gain access to certain foods (just as they can be
used to scratch hard to reach places on the back), but they did not
evolve as a response to these tasks.

We now arrive at a series of theories that actually tie together
under the umbrella of ‘social apparatus’. The most widely regarded
explanation for the evolution of antlers is that they may be both an
advertisement of fitness (both to females and other males) and weapons
for use in intraspecific combat (i.e. between members of the same
species). In his 1998 book, Deer of the World, Valerius Geist argued
that antlers evolved as a response to feeding out in the open; being out
in the open makes you more vulnerable to predators, which permits the
formation of herds because more eyes and ears makes it less likely any
one individual is going to get attacked. The downside to living in a
group is that there are many mouths going for the same food, in other
words there’s competition, and this leads to aggression and in-fighting.
Now, as Dr Geist elucidated:

“Weapons that maximize wounding ultimately attract predators to the
group, disrupt normal functions, and increase the cost of daily living
to the group. Statistically, an individual that leaves the group due to
wounds or fright reduces the security of each individual remaining in
the group.”

So, animals living in a herd need a way of establishing a ‘pecking
order’ without causing any serious injury – complex antlers do just
this, by allowing largely ‘bloodless’ wrestling and sparring matches. The antlers serve to catch the charge of an opponent and hold onto his
head so that wrestling can commence. Geist gives a detailed coverage
of the evolution of antler forms and the reader is directed there for a
more complete picture, but suffice to say that the precursors to modern
antlers (so-called protoantlers) were bony, skin-covered, hairy
extensions of the skull possessed by the mid-Miocene deer Dicroceros
elegans and used in defence (curved upper canines were the offensive
weapons). These protoantlers probably evolved into bony lumps on the
head as a response to a need for protecting the head against bites.
According to Geist, it was the bone protecting the underlying skull
structure that was the origin of the early true antlers; such antlers
are first recorded on small deer from Old World Europe that looked
similar to modern day muntjac. (Photo:
Fallow buck with antler buds.)

Of course, competition for food is not the only form of contest that
herding animals experience; competition for mates is equally important
and antlers appear to have evolved to allow males to compete with each
other for access to females. Indeed, as Dr Clutton-Block noted in his
review: “The occurrence of antlers in males and their absence in females
(who do not have to fight for access to mating partners) is in
accordance with the theory that they evolved as weapons.” So, can we
prove that antlers are primarily used as weapons for intraspecific
competition? Yes, by experimentally removing the antlers of captive
deer. Many such experiments were carried out by Gerald Lincoln during
the late 1960s and early 1970s and the results showed that when antlers
were removed, the stags fell to the bottom of the hierarchy – the
antlerless stags were challenged immediately by other members of the
group. Similar observations were made by Michael Abbleby working with
Red deer in Scotland and by Ludek Bartos and Vaclav Perner on the white
Red deer herd kept on the Zehusice Game Reserve in Czechoslovakia. Red
stags form bachelor groups outside of the breeding season and these
scientists reported that as the stags cast their antlers they rapidly
dropped in the hierarchy; once all the deer had cast, the pecking order
was reinstated. A loss of status seems to correspond to poor breeding
success in wild populations, because without antlers the males cannot
compete with other antlered males and thus fail to maintain a harem. In
a paper to the Journal of Experimental Zoology during 1972, Dr Lincoln
wrote:

“... the loss of antlers can radically impair the rutting performance,
and prevent animals from taking a harem and participating in mating ...”

The relationship between antler size and fighting ability or
dominance is less clear. Some authors, such as Clutton-Brock in his
Behaviour review, point out that the relationship between antler size
and dominance is not a particularly close one and an individual’s
fighting ability changes throughout the rutting season, while his antler
size remains constant. There are, however, multiple studies confirming a
positive correlation between antler size and body size so if, as the
studies suggest, body size is the major factor influencing rutting
success some have argued that it should be possible to gauge a stag’s
fighting prowess based on his antler size. There is some evidence, from
a study using stuffed heads with different antler sizes, that stags can
do this, but Clutton-Brock considers that a stag basing a decision
whether or not to fight another based solely on its antlers is likely to
make the wrong choice. In the 1982 book, Clutton-Brock and his
colleagues point out:

“... among stags over five years old in our study area, neither fighting
success nor reproductive success was related to antler length ...”

Indeed, Clutton-Brock questions whether correlations between
antler size and dominance, fighting ability and reproductive success are
picking up on a relationship that is actually a by-product of the well
known correlation between body size and dominance. This would make sense
given that antler breakage doesn’t seem to have any significant impact
on rutting performance. In a study of the Tule elk (Cervus cannadensis
nannodes), for example, California Fish and Game biologist Heather
Johnson and her colleagues found that antler breakage, regardless of
severity, had no effect on either the fighting success or harem-holding
success of bull elks in Owens Valley, California. Even if breakage were
a problem, it appears to be rare and, in a 1971 note to the journal
Nature, John Henshaw wrote of how he had only come across one instance
of breakage of the main beam in his observations of “approximately a
quarter of a million cervids of nine species”. We still cannot be sure
what visual cues females use when assessing a potential mate, or that
stags use when assessing a potential challenger, but it is thought that
antler size may be part of the story, providing a ‘by proxy’ clue.

Deer use their antlers to settle
disputes. During the rut, as males compete for access for females, these
Fallow bucks lock antlers and try to push each other back. The winner is
the deer that manages to push the other one back, forcing a hasty
retreat.

In 2005 a team of Spanish biologists lead by Aurelio Malo at the
Museo Nacional de Ciencias Naturales in Madrid found that Red stags
sporting large, complex antlers had relatively larger testes and faster
sperm than those with smaller, simpler appendages. Subsequently, in a
2007 paper to The American Naturalist, a team of French and Swedish
scientists argued that antler size may “provide an honest signal of male
phenotypic quality in roe deer” – in other words, Roe does may be able
to tell the quality of a male by the size of his antlers. Thus, females
may be able to use the size of a stag or buck’s antlers as a cue to
their quality as a mate, because large antlers generally indicate a buck
in good condition, that is, a fit buck. If females then actively chose
males with large, complex antlers over those with smaller, simpler ones
then there would be a selective pressure towards males with large and
complex ornaments. Data from the Rum population provide some evidence
for this, showing that the mating success of stags between the ages of
seven and ten years is associated with the number of points on their
antlers -- those with more points generally have more matings that those
with fewer points -- although the relationship is not always clear.

Studies on the mechanical properties of antler bone have lent
additional support to the theory that they evolved primarily as weapons. A study by University of York biologist John Currey and his colleagues
assessed how effective antler of varying ‘moistness’ was at standing up
to force. The researchers compared various measures of physical strength
(elasticity, work-to-fracture ratio, etc.) of antler samples and sections
of wet femur; they discovered that antler could withstand almost
two-and-a-half times more sustained force (i.e. force attempting to bend
the antler to breaking point) and six-and-a-half times more blunt impact
force than wet femur before it broke. The biologists suggested that the
antlers begin to dry out once the velvet is shed, but only sufficient
moisture is lost to improve the mechanical properties of the bone. Thus,
if the antler was too wet it would simply distort under the pressure
applied during a clash, but if it were too dry it would be stiffer, more
brittle and thus more likely to break. Indeed, Richard Prior points to a
similar scenario in his 1995 book, suggesting that Roe antlers gain
density, perhaps by absorbing resins and so on through fraying –
Prior points out that most late-shot bucks seem to have very hard, dense
antler compared with those shot just out of velvet, implying a gradual
drying out of the antlers following casting. (Photo:
A Roe deer buck in his winter coat and with antlers in velvet. Roe are
unusual among deer in growing their antlers during the winter.)

Before we leave the subject of what use antlers may serve, it is
worth briefly mentioning work by University of Guelph biologist George
Bubenik and Cleveland State University mathematician Peter Bubenik. In a
2008 paper to the European Journal of Wildlife Research these scientists
presented data showing that the palmated (broad, flat) antlers of
Alaskan moose (Alces alces) might serve as a parabolic reflector of
sound. The researchers constructed a ‘fake ear’ and attached it to an
antler, pointing it at various different angles. The data showed that
the loudest response was registered when the ear was facing the centre
of the antler; the sound pressure was 119% that of when the ear was
facing forwards (i.e. away from the antler). The authors wrote:

“These findings strongly indicate that the palm of moose antlers may
serve as an effective, parabolic reflector which increases the acoustic
pressure of the incoming sound”

Some researchers have suggested that
large, flat, palmate antlers may serve to funnel sound into the
ears of their owner (a bull moose, above), improving the deer's ability
to locate sound sources.

In other words, the sound hits the antler and is bounced off into the
ear, thereby improving the moose’s hearing. It seems unlikely that
antler evolved in moose in response to a need for better hearing, but it
reinforces the idea that such structures may convey more advantages than
we might initially realise.

Not all antlers grow and develop in the pattern typical of the
species. Sometimes aberrations occur, including atypical antler growth
in female deer.

Abnormalities and curiosities
Perhaps one of the most curious aspects
of antler biology is when they are grown by animals that don’t generally
grow them, or when animals that should normally grow them fail to do so.
We have already seen that female Reindeer grow antlers, but they have
been documented in other deer too. Most frequently such reports come
from Roe deer and, as Richard Prior alludes to in his The Roe Deer book,
it is not unusual for older females to possess antlers. Prior
explains:

“Old does quite commonly grow short antlers in velvet, usually not
more than five centimetres long. They are normal breeders, but probably
towards the end of their reproductive life.”

Prior goes on to recount the story of a doe he hand-reared, which
developed antlers in velvet from the age of eight; the antlers grew
larger in successive years (lengthening to 15cm / 6 in.) and by the time
she died, the doe had developed an abnormality called ‘perruque head’
(see below). A post mortem of the doe revealed some testicular cells in
the vicinity of her ovaries. Indeed, the development of antlers in
female deer typically seems to be related to a hormonal imbalance, which
appears to occur in old age. Alternatively, it may be that the
testicular cells may always be present, but their influence is
overpowered by the oestrogens secreted by the ovaries – as the doe ages,
perhaps a drop in oestrogen secretion allows testosterone to have an
influence. Either way, in their 2008 review of Roe Deer natural history
Mark Hewison and Brian Staines note that antlers in does are often
associated with hermaphroditism, both ‘true’ (where both male and female
genital tissue is present) and ‘pseudo’ (where one sex displays the
sexual organs of the other). The biologists also point out that pregnant
antlered Roe deer are known and that, although doe antlers generally
fail to shed velvet, does in ‘hard horn’ have been reported. Roe are not
the only species in which females can uncharacteristically grow antlers
– in White-tailed deer, for example, antlers are estimated to occur in
roughly 0.1% (i.e. 1 in every 1000) of females. (Photo:
Mule deer, Odocoileus hemionus, that has failed to shed the
velvet on his right antler.)

In some cases, stags and bucks fail to develop antlers – such deer
are called hummels or, in parts of south-west England,
notts. Early theories proposed that the lack of antlers
was either the result of accidental damage to the testicles, or that it
was a heritable genetic condition (i.e. hummels bred to produce hummels). It should be noted, at
this point, that true hummels are distinct from haviers -- which are
antlerless as a result of castration -- and that, although lacking
antlers, they are fertile. Some stalkers believed that hummels were
actually at an advantage over antlered stags because, spared the drains
of antler development, they could grow larger and would therefore be
more successful in obtaining a harem during the rut. Consequently,
hummels tended to be shot on sight in a bid to improve the local trophy
standards. In a paper to the Deer journal during 1970,
however, Brian
Mitchell and Tim Parish presented data showing that hummels do not
necessarily grow larger than antlered stags, while the studies by Gerald
Lincoln discussed earlier have demonstrated that antlerless stags are at
a disadvantage during the rutting season. Our understanding of hummels
took a sizeable step forward when a ‘congenitally polled’ (polled means
‘without horns’) Red stag was caught at Braemar Lodge in the Scottish
Highlands during 1969. Breeding studies conducted by Gerald Lincoln and
John Fletcher clearly demonstrated that the hummel condition was not
genetic – the stag sired multiple antlered progeny, which also sired
antlered stags even when crossed with their sisters (ruling out a
recessive gene). This stag also provided scientists with a better
understanding of what causes the lack of antlers in hummels.

In 1974, Polish anatomists Zbigniew Jaczewski and Krystyna Krzywinska
reported that amputation of the tip of the pedicle of a castrated stag
would sometimes cause it to grow an antler, as if the act of wounding
the pedicle was the stimulation for antlerogenesis. In a 1976 paper to
the Journal of Experimental Zoology, Gerald Lincoln and John Fletcher
presented the results of their surgical study on the Braemar Lodge
hummel, which had “rudimentary pedicles” but failed to grow antlers from
them during five years of observation. The biologists found that if they
amputated the tip of the stag’s right pedicle, the deer grew a complete
(albeit stunted) antler on this side (no growth was documented on the
left pedicle), which was subsequently cleaned and then cast in the
normal way. The stag died shortly after the experiment and dissection
revealed a substantial increase in the thickness of the right pedicle
compared to the left. Lincoln and Fletcher concluded that hummels
weren’t physiologically incapable of producing antlers; instead a
failure to develop fully formed pedicles meant that the antlers had no
base from which to differentiate. The researchers wrote:

“... it was possible to induce antler growth in the hummel by apparently
simulating the process of ‘wounding’ that naturally occurs at the time
of antler casting.”

Skull of the Braemar Lodge hummel,
showing a hypertrophied right pedicle (circled) following surgical
wounding. Photo used with permission.

In other words, it may be the wounding of the pedicle caused when the
antler is cast that, in conjunction with a drop in testosterone
secretion, triggers the growth of the antler. So, why might stags fail
to develop normal pedicles? Lincoln and Fletcher suggest that, given
most hummels are found among the Red deer of the Scottish hillsides,
they may come about under conditions of low food availability; low
nutrient levels experienced as a calf may starve the pedicles of the
minerals needed during a crucial growth period. Alternatively,
researchers at the Croatian Forestry Society in Zagreb proposed, in a
2008 paper to the Croatian journal Sumarski List, that:

“As pedicle growth depends on androgenic [testosterone] stimulation,
low levels of circulating androgens or a low density of androgen
receptors in the antlerogenic periosteum could lead to poor pedicle
growth and in consequence to a complete or almost complete lack of
antler growth.”

Hummels are relatively rare (in 1990, G. Kenneth Whitehead put the
figure at less than 1% of Scottish Red deer), so the data we have are
from only a few individuals and the results may not be representative of
all cases. However, off-hand it seems that, if the hummels were a
response to a lack of androgen receptors in the pedicle, this is
unlikely to be corrected by simple surgical wounding of the tissue.
Ultimately we are still unsure as to the exact cause of this condition,
but it seems likely that both early malnutrition and abnormally low
testosterone levels are possible contenders. It should be mentioned,
incidentally, that although hummels appear more common in Red deer than
other species, it is not a condition unique to Cervus elaphus; there are
occasional records of Roe bucks without antlers.

Antler deformities come in various shapes and sizes and, although
none are particularly common, they are typically associated with
hormonal imbalances. In her 1991 book, Deer, Norma Chapman notes that
the so-called double-head condition is well known in Fallow bucks from
Denmark and Germany, with rare reports in German Roe deer and Scottish
Red deer. The condition manifests as either a failure to cast the
antlers before the new set begin growing, leading to four antlers being
present simultaneously from two pedicles, or the formation of an
additional one or two pedicles on the skull from which antlers will
grow. The phenomenon of failing to cast before new growth begins can
take a more serious turn in a compound-growth condition known as perruque. Perruque, from the French meaning ‘wig’, is a condition where
the antlers continue to grow during subsequent years without casting;
the result is the growth of what can, in advanced cases, be a rather
grotesque and heavy lump of bone that cascades down across the face and
obscures the eyes. In particularly warm periods any damage to the velvet
tissue, which is often retained indefinitely, may become infected.
Perruque seems to be caused by damage to the testicles. To the best of
my knowledge, the only documentation of the onset and progress of
perruque in Roe deer comes from this single Roe Prior cared for.
Although most commonly reported in Roe bucks, there are occasional
records of less dramatic perruqueing in Fallow and Red deer.

Roe bucks have been recorded with coalesced antlers (see
right), where
the main beams merge into a single thick mass; they are shed as a single
unit. Coalescence seems to be the result of larger, thicker pedicles
being situated closer together than normal; in his 1995 book, Prior
notes that this condition may be more common in elderly bucks, as the
pedicles thicken and shorten with successive antler castings. Injuries
to limbs have also been implicated in the abnormal development of
antlers. There are surgical experiments in Sambar (Cervus unicolor) and
Indian muntjac (Muntiacus muntjak) deer showing that amputation of part of one
hind limb can lead to stunted growth of the opposite antler – amputation
of the left hind leg, for example, would produce stunted growth of the
right antler. In his Encyclopedia of Deer, Whitehead suggests that
this may be a form of ‘bilateral compensation’, recounting a case where
a Sambar deer grew a left antler three-to-four times heavier than the
right, apparently to compensate (balance out) a weakened, handicapped
left hind leg. Similar stories are discussed by John Fletcher in his
A
Life for Deer, in which he tells how deer stalkers long spoke of how an
injured stag would “grow a twisted horn”. Fletcher mentions that,
although deer have an extraordinary capacity to repair bone fractures
spontaneously, where a fracture coincides with antler growth an
asymmetrical antler with distorted growth is almost inevitable; he
speculates that this might be related to liberation of endorphins
(natural pain killing chemicals) by the body.

Hormones tend to be involved in antler abnormalities in one form or
another, but in some cases parasites have been implicated. There are
some rare examples of deer (generally Red stags) growing twisted, or
corkscrew, antlers; the origin of such abnormalities is currently
unknown, but it has been suggested that it may be related to internal
parasite -- specifically lungworm (Dictyocaulus spp.) -- load.

So, in summary we have established that antlers are deciduous bony
structures that develop from extensions of the stag’s (and in some
species, hind’s) skull. The first antlers are usually simple, unbranched
spikes that grow as extensions to the pedicle and thus lack a coronet;
subsequent antlers become progressively larger and more branched.
Casting and re-growing of the antlers is under seasonal influence, which
acts upon androgen levels in the deer’s blood – in spring, low
testosterone levels cause the antlers to be cast and new growth to
start, while in the autumn a rise in testosterone (in preparation for
the rut) causes the velvet to be shed. There are times when antler
development goes awry and these are generally associated with hormonal
imbalances, as are the atypical growth of antlers in females. Antlers
are used as weapons during combat between stags for mating rights and,
in reindeer, may help find food buried under the snow and compete with
bulls for access to precious winter resources. (Back to
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